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Introduction. In the structure of the total mortality of the population, cerebral stroke ranks second and leads among the causes of disability. Despite the huge number of patients with diabetes and stroke, the mechanisms underlying this predisposition remain poorly understood. Morphological changes of the brain in diabetes-induced neuroinflammation are practically not described anywhere.Objective. To establish the patterns of pathomorphological changes of the brain associated with neuroinflammation in patients with type 2 diabetes mellitus who have suffered a stroke.Materials and methods. On the sectional material, changes in the brain and arteries were studied in 27 stroke deaths (6 men and 21 women), aged 60 to 97 years, average age 75 ± 7.2 years, who had type 2 diabetes mellitus, the comparison group consisted of 32 stroke deaths (14 men, 18 women) with dyscirculatory encephalopathy without type 2 diabetes aged 42 to 100 years (average age 68.5 ± 14.2 years). Light-optical and electron microscopic examination of the brain, immunohistochemical reactions were performed: indirect immunoperoxidase reaction with gliofibrillary protein, vimentin and macrophage immunophenotyping markers – CD-68, CD-163, CD-21, CD-23, CD-11c, HAM.Results. It has been established that neuroinflammation is characterized by macrophage-microglial activation, penetration of antigen-presenting cells through the damaged blood-brain barrier, damage to neuronal and glial cell pools. Pronounced macrophage infiltration was revealed using immunohistochemical methods of investigation with CD-68. Monocytic macrophages and antigen-presenting cells are located perivascularly, migrating through the damaged blood-brain barrier and expressing the CD-11c receptor. There is a phenomenon of changing the phenotype of macrophages from M2-type, with sanogenetic activity, to M1-type, responsible for inflammatory damage.Conclusions. Pronounced infiltration of brain tissue in stroke patients with type 2 diabetes mellitus by both resident macrophages and monocytic macrophages is associated with progressive neuroinflammation.

In vitro differentiation of donor blood monocytes to macrophages (Mph) following GM-CSF treatment was accompanied by a significant increase in the levels of gene transcription signaling receptors TLR7 or RIG1. The levels of intracellular viral RNA (M1 gene) in Mph remained high upon infection by influenza virus A H1N1pdm (Moscow 2009) for 24-96 hours. The innate immunity reactions caused by influenza virus show individual features: they are decreased in Mph from donor 1 which had initially high level of endosomal TLR7 gene activity, and it increased by influenza virus in MPh from donor 2 who had a very low level of TLR7 gene expression. The influenza H1N1pdm virus weakly stimulated expression of gene RIG1 and production of inflammatory cytokines in Mf in donor 1. The differences may be connected with individual sensitivity of the donors to influenza infection.